Melanomas resist treatments by breaking genes

by time news

2024-04-12 15:10:00

He melanomathe most lethal form of skin cancer, represents a significant challenge to medical science as global incidence rates continue to rise.

In the search for more effective treatments, recent advances point to the use of genetic tests to identify specific mutations in order to design a personalized therapy that can provide a solution to the increasing number of cases.

Unfortunately, as explained by a Spaniard who studied at the Center for Genomic Regulation (CRG) in Barcelona, ​​he reveals unflattering information: melanomas have the ability to outwit medications. As? Breaking the genes.

“Melanoma drug resistance is an imminent threat, affecting almost all patients with BRAF mutations who are receiving targeted therapy,” he says. Francisco Aya Moreno. Therefore, he emphasizes, it is urgent to understand the mechanisms behind this resistance.

Research published in Cell Reports uncovers a novel mechanism by which melanomas outperform treatment strategies.

What the research reveals is that cancer cells, in response to treatments, have a mechanism that is capable of fragmenting segments of their BRAF gene, a crucial target for cancer inhibition.

The researchers explain in their work that this fragmentation, called genomic deletions, allows the tumor to generate alternative versions of the BRAF protein, called altBRAFswhich prevent the effects of BRAF inhibitors, thus reactivating cancer growth pathways.

What is even more alarming is that these genomic deletions appear to occur even before the start of treatment, hinting at a pre-existing ability within melanomas to mimic drug resistance.

This finding underscores the importance of comprehensive genetic profiling before treatment, potentially revolutionizing the efficacy of initial therapeutic interventions.

Other cancers

Furthermore, the study’s implications extend beyond melanoma. Evidence for similar genomic deletions and altBRAFs has been found in other cancer types, including non-small cell lung cancer, breast cancer, kidney cancer, and prostate cancer. This suggests a broader application for targeted treatments, offering hope for patients in various malignancies.

Moreno advocates for the inclusion of diverse patient cohorts in clinical trials for second-generation RAF inhibitors, which exhibit a broader spectrum of action and could potentially counteract altBRAF activity.

This expanded approach could mark a significant progress in the battle against resistant cancers to medications.

The study not only uncovers the mechanics of melanoma resistance, but also underscores the invaluable synergy between clinical insight and scientific research.

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